L23 - regulation of food intake Flashcards
(19 cards)
what is glucoses role in the body
- glucose is the principal circulating sugar in the blood and the major energy source of the body
- glucose metabolism maintains blood glucose levels at 4-6 mM
describe the energy stores form glucose
glycogen is the energy storage molecule and it is just a bunch of glucose molecules bonded together in a highly packed structure that can be stored for when its needed
describe energy stores from fatty acids
glycerol + three fatty acids —(dehydration)—-> triglyceride (fat) (energy storage molecule)
if you take on too much glucose it will be stored as fat
if your glycogen fuel stores run low enough you will start to break down/burn more fat
describe protein anabolism
anabolism is making things
if you run out of normal healthy energy stores (glycogen and fat) you will start breaking down proteins to make energy
Absorptive state (Anabolic: high insulin)
- have just eaten something, so the principal thing to do is get it into the bay and use it
- most cells will use glucose in this state, if extra glucose it will be stored (making stores)
Over the course of 4 hours switch into the postabsorptive state (catabolic: low insulin)
- reversing energy storage molecules to the molecules that can be used
- brain can only use glucose!
- all the other substrates get converted to glucose in the liber and can be released to become available as the energy source
all controlled by the pancreas
describe the endocrine pancreas (exocrine and endocrine portions)
- exocrine (98%) and endocrine (2%) portions
- endocrine portions consisted of 1-3 million islets of Langerhans (pancreatic islets)
- B (beta) cells secrete insulin, A (alpha) cells secrete glucagon
- 60-80% of cells within Islets are B cells
exocrine - secretes outside the body (GIT included as outside the body)
endocrine - secretion into the body
what is the structure of insulin
A chain, B chain and C peptide
- C peptide is cleaved off but still secreted with the insulin, hence can measure C peptide levels to determine a diabetics natural insulin levels
- insulin is a peptide hormone, secreted by exocytosis bc can’t cross the cell membrane to physically get anything inside the cell
describe the structure of the insulin receptor and what each aspect does (diagram on slides)
- homodimer: two identical units, each with an alpha and beta subunit
- alpha subunits: extracellular, insulin binding
- beta subunits: intracellular, signal transduction
- beta subunits autophosphorylate tyrosine and then phosphorylate insulin receptor substrates
this is a tyrosine kinase receptor, not a G-protein coupled receptor
what are the cellular effects of insulin
- insulin receptor activation
- results in exocytosis so that glucose transporters can get onto the cell surface
- facilitated diffusion of glucose
- endocytosis to remove glucose transporters
- recycling of transporters and other molecules for the next round
insulin secretion results in increased glucose transporters in the cell membrane
if insulin levels go down then you don’t get repetition of this cycle ?
describe the control of insulin secretion
- increased plasma glucose
- pancreatic isla beta cells: increased insulin secretion
- increased plasma insulin
- adipocytes: increase glucose uptake, liver: cessation of glucose output, net glucose uptake
- restoration of plasma glucose to normal
describe glucagon and glucose metabolism
- insulin is the only regulator that decreases blood glucose levels
- if blood glucose levels drop too low, glucagon increase glucose release from cellular stores
- glucagon is a peptide hormone produced by alpha cells in the islets of langerhans (pancreatic islets) that opposes insulin actions to:
1. increase glycogenolysis (liberating glucose)
2. increase gluconeogenesis (synthesising glucose)
describe post-prandial insulin and glucagon secretion
as you go from the absorptive to post-absorptive phase you get an increase in glycogen (primary backup) and slight decrease in insulin
describe obesity as a major health problem
- over 30% of adults and over 10% of children in NZ are classified as obese by body mass index
- obesity is a risk factor for many chronic diseases, including type 2 diabetes, heart disease, high blood pressure, stroke, gallstones and some cancers
- more than 1000 NZers die each year from obesity-related diseases - more than double the annual road toll
it is not a lifestyle choice:
- genes: monogenic syndromes and susceptibility genes
- environmental factors: metabolic rate, excersise, food intake, culture
all play a major role in obesity
describe the factors that regulate food intake
lots of signals to the brain, but the most important for long-term regulation of bodyweight are increased plasma leptin (signals full) and increased plasma ghrelin (signals hungry)
describe leptin: the ob/ob mouse
- peptide hormone secreted by fat (adipose cells)
- product of the ob gene that has 67% sequence identity across species
- mutations in the ob gene are not common in humans
- no evidence of an association between polymorphisms in the leptin gene (or leptin receptor gene) and obesity
how is leptin secretion controlled
- energy intake > energy expenditure
- adipose tissue: increased fat deposition, which leads to increased leptin secretion
- increased plasma leptin concentration
- hypothalamus: altered activity of integrating centres
- decreased energy intake, increased metabolism rate
negative feedback loop
describe grhelin
- peptide hormone ‘hunger hormone’
- secreted by X/A like cells in the oxyntic glands of the stomach
- stimulates: hunger, food intake, gastric emptying
- suppresses fat utilisation in adipose tissue
- ghrelin concentrations in blood are low in obese humans (not known why)
ghrelin levels spike just before each meal (because you it makes you hungry so then you eat)
describe the central regulation of food intake (diagram on slides)
grhelin acts on orexigenic which activates integrator to get food intake and energy expenditure ?
leptin acts on anorexigenic which negatively affects the integrator ?
blood leptin levels are relatively constant so grhelin overtakes it to make you hungry and then once you have eaten the ghrelin levels die back down and leptin becomes more prominent (even though its level hasn’t changed)
what are some recent advances in obesity therapies
glucagon-like peptide-1 and gastric inhibitory polypeptide drugs
- suppresses hunger, stimulates insulin release, suppresses glucagon secretion, slows gastric emptying, increases fatty acid and glucose uptake by fat tissue
describe energy balance
- conventional wisdom holds that obesity is caused by over-indulgence in fatty or sherry goods
- BUT.. a professor said ‘as long as your expenditure equals what you eat, you won’t put on weight, regardless of how high the fat content is in your diet’
- despite the increased evidence of childhood obesity, most children eat less than children of previous generations
